Marie Potier-Cartereau

Dr. Marie Potier-Cartereau

orcid

Research Focus & Metrics

Academic Career Length

34Years (1993-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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18 April 2016 in Oncotarget
Verified
Journal Article
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MGMaxime Guéguinou
Maxime Guéguinou
THThomas Harnois
Thomas Harnois
DCDavid Crottes
David Crottes
AUArnaud Uguen
Arnaud Uguen
NDNadine Deliot
Nadine Deliot
MPMarie Potier-Cartereau
Marie Potier-Cartereau
SK3/TRPC1/Orai1 complex regulates SOCE- dependent colon cancer cell migration: a novel opportunity to modulate Anti- EGFR mAb action by the alkyl-lipid Ohmline

12 February 2020 in Cells
Verified
Journal Article
Open access
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CDCéline Delierneux
Céline Delierneux
SKSana Kouba
Sana Kouba
SSSanthanam Shanmughapriya
Santhanam Shanmughapriya
MPMarie Potier-Cartereau
Marie Potier-Cartereau
Mohamed TrebakMohamed Trebak
Mohamed Trebak
NHNadine Hempel
Nadine Hempel
Calcium (Ca2+) uptake into the mitochondria shapes cellular Ca2+ signals and acts as a key effector for ATP generation. In addition, mitochondria-derived reactive oxygen species (mROS), produced as a consequence of ATP synthesis at the electron transport chain (ETC), modulate cellular signaling pathways that contribute to many cellular processes. Cancer cells modulate mitochondrial Ca2+ ([Ca2+]m) homeostasis by altering the expression and function of mitochondrial Ca2+ channels and transporters required for the uptake and extrusion of mitochondrial Ca2+. Regulated elevations in [Ca2+]m are required for the activity of several mitochondrial enzymes, and this in turn regulates metabolic flux, mitochondrial ETC function and mROS generation. Alterations in both [Ca2+]m and mROS are hallmarks of many tumors, and elevated mROS is a known driver of pro-tumorigenic redox signaling, resulting in the activation of pathways implicated in cellular proliferation, metabolic alterations and stress-adaptations. In this review, we highlight recent studies that demonstrate the interplay between [Ca2+]m and mROS signaling in cancer.

1 July 2019 in Cell Calcium
Verified
Journal Article
Closed access
SKSana Kouba
Sana Kouba
LOLobna Ouldamer
Lobna Ouldamer
CGCéline Garcia
Céline Garcia
DFDelphine Fontaine
Delphine Fontaine
ACAurélie Chantome
Aurélie Chantome
MPMarie Potier-Cartereau
Marie Potier-Cartereau

11 November 2022 in Cell Calcium
Verified
Journal Article
Closed access
OROlivier Romito
Olivier Romito
Maxime F. GuéguinouMaxime F. Guéguinou
Maxime F. Guéguinou
WRWilliam Raoul
William Raoul
OCOphélie Champion
Ophélie Champion
ARAlison Robert
Alison Robert
MPMarie Potier-Cartereau
Marie Potier-Cartereau

Verified
Journal Article
Open access
PDF file
FBFanny Bery
Fanny Bery
SFSandy Figiel
Sandy Figiel
SKSana Kouba
Sana Kouba
DFDelphine Fontaine
Delphine Fontaine
Maxime F. GuéguinouMaxime F. Guéguinou
Maxime F. Guéguinou
KMKarine Mahéo
Karine Mahéo
Hypoxia is a well-established feature of prostate cancer (PCa) and is associated with disease aggressiveness. The hypoxic microenvironment initiates multiple adaptive responses including epithelial-to-mesenchymal transition (EMT) and a remodeling of calcium homeostasis involved in cancer progression. In the present study, we identified a new hypoxia signaling pathway with a positive feedback loop between the EMT transcription factor Zeb1 and SK3, a Ca2+-activated K+ channel, which leads to amplifying store-operated Ca2+ entry. Zeb1 and SK3 channel were strongly upregulated by hypoxia both in vitro and ex vivo in organotypic cultures of human PCa. Taking into account the sensitivity of the SK3 channel to the membrane lipid composition, we identified lipids such as Ohmline (an alkyl ether lipid and SK3 inhibitor), linoleic acid (LA) and eicosapentaenoic acid (EPA) (fatty acids associated with indolent PCa), which were able to completely abrogate the hypoxia-induced changes in Zeb1 expression. Ultimately, better understanding of this new hypoxia-induced EMT pathway may allow to develop adjuvant therapeutic strategies, in order to control PCa aggressiveness and improve treatment outcomes.

18 November 2019 in Cancers
Verified
Journal Article
Open access
PDF file
SFSandy Figiel
Sandy Figiel
FBFanny Bery
Fanny Bery
ACAurélie Chantôme
Aurélie Chantôme
DFDelphine Fontaine
Delphine Fontaine
CPCôme Pasqualin
Côme Pasqualin
KMKarine Mahéo
Karine Mahéo
The composition of periprostatic adipose tissue (PPAT) has been shown to play a role in prostate cancer (PCa) progression. We recently reported an inverse association between PCa aggressiveness and elevated PPAT linoleic acid (LA) and eicosapentaenoic acid (EPA) content. In the present study, we identified a new signaling pathway with a positive feedback loop between the epithelial-to-mesenchymal transition (EMT) transcription factor Zeb1 and the Ca2+-activated K+ channel SK3, which leads to an amplification of Ca2+ entry and cellular migration. Using in vitro experiments and ex vivo cultures of human PCa slices, we demonstrated that LA and EPA exert anticancer effects, by modulating Ca2+ entry, which was involved in Zeb1 regulation and cancer cellular migration. This functional approach using human prostate tumors highlights the clinical relevance of our observations, and may allow us to consider the possibility of targeting cancer spread by altering the lipid microenvironment.